Tau in Alzheimer’s Disease:Pathological Alterations and an Attractive Therapeutic Target  

作　　者：Jian-lan GU Fei LIU 

机构地区：[1]Department of Biochemistry and Molecular Biology,School of Medicine,Nantong University,Nantong 226001,China [2]Key Laboratory of Neuroregeneration and Ministry of Education of Jiangsu,Co-innovation Center of Neuroregeneration,Nantong 226001,China [3]Department of Neurochemistry,Inge Grundke-Iqbal Research Floor,New York State Institute for Basic Research in Developmental Disabilities,Staten Island,NY 10314,USA

出　　处：《Current Medical Science》2020年第6期1009-1021,共13页当代医学科学（英文）

基　　金：This project was supported by National Natural Science Foundation of China(No.31870772).

摘　　要：Alzheimer’s disease(AD)is an age-related neurodegenerative disease with two major hallmarks:extracellular amyloid plaques made of amyloid-β(Aβ)and intracellular neurofibrillary tangles(NFTs)of abnormally hyperphosphorylated tau.The number of NFTs correlates positively with the severity of dementia in AD patients.However,there is still no efficient therapy available for AD treatment and prevention so far.A deeper understanding of AD pathogenesis has identified novel strategies for the generation of specific therapies over the past few decades.Several studies have suggested that the prion-like seeding and spreading of tau pathology in the brain may be a key driver of AD.Tau protein is considered as a promising candidate target for the development of therapeutic interventions due to its considerable pathological role in a variety of neurodegenerative disorders.Abnormal tau hyperphosphorylation plays a detrimental pathological role,eventually leading to neurodegeneration.In the present review,we describe the recent research progresses in the pathological mechanisms of tau protein in AD and briefly discuss tau-based therapeutic strategies.

关 键 词：Alzheimer’s disease tau protein HYPERPHOSPHORYLATION propagation of tau pathology 

分 类 号：R74[医药卫生—神经病学与精神病学]